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Apoptosis caused by p53-induced protein with death domain (PIDD) depends on the death adapter protein RAIDD.


ABSTRACT: The p53 tumor suppressor promotes cell cycle arrest or apoptosis in response to diverse stress stimuli. p53-mediated cell death depends in large part on transcriptional up-regulation of target genes. One of these targets, P53-induced protein with a death domain (PIDD), was shown to function as a mediator of p53-dependent apoptosis. Here we show that PIDD is a cytoplasmic protein, and that PIDD-induced apoptosis and growth suppression in embryonic fibroblasts depend on the adaptor protein receptor-interacting protein (RIP)-associated ICH-1/CED-3 homologous protein with a death domain (RAIDD). We provide evidence that PIDD-induced cell death is associated with the early activation of caspase-2 and later activation of caspase-3 and -7. Our results also show that caspase-2(-/-), in contrast to RAIDD(-/-), mouse embryonic fibroblasts, are only partially resistant to PIDD. Our findings suggest that caspase-2 contributes to PIDD-mediated cell death, but that it is not the sole effector of this pathway.

SUBMITTER: Berube C 

PROVIDER: S-EPMC1242316 | biostudies-literature | 2005 Oct

REPOSITORIES: biostudies-literature

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Apoptosis caused by p53-induced protein with death domain (PIDD) depends on the death adapter protein RAIDD.

Berube Christina C   Boucher Louis-Martin LM   Ma Weili W   Wakeham Andrew A   Salmena Leonardo L   Hakem Razqallah R   Yeh Wen-Chen WC   Mak Tak W TW   Benchimol Samuel S  

Proceedings of the National Academy of Sciences of the United States of America 20050923 40


The p53 tumor suppressor promotes cell cycle arrest or apoptosis in response to diverse stress stimuli. p53-mediated cell death depends in large part on transcriptional up-regulation of target genes. One of these targets, P53-induced protein with a death domain (PIDD), was shown to function as a mediator of p53-dependent apoptosis. Here we show that PIDD is a cytoplasmic protein, and that PIDD-induced apoptosis and growth suppression in embryonic fibroblasts depend on the adaptor protein recepto  ...[more]

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